Hepatic encephalopathy

Hepatic encephalopathy (HE) is a neurocognitive disorder that is associated with both acute and chronic liver injury. It has grown to become a dynamic syndrome, spanning a spectrum of neuropsychological impairment from normal performance through to coma. In acute liver failure, the central role of ammonia in the development of brain oedema remains incontrovertible but over the past 10 years, hepatologists have begun to characterize the key roles of precipitating factors, such as inflammation, infection and hyponatraemia, in modulating the pathophysiological effects of ammonia on the brain, particularly in patients with cirrhosis. This article explores the current thoughts and evidence base in this area and the potential role of existing therapies such as lactulose, and newer therapies such as rifaximin, which may abrogate systemic inflammation in patients with, or at risk of developing HE. The development of HE is often unpredictable and its management, particularly in a ward environment, remains challenging and patients frequently require augmented levels of care in a high-dependency or intensive care arena. The probability of maintaining a transplant-free survival after a first episode of HE at 3 years is only 23% and therefore referral for liver transplantation should be considered early.